Our experiments use two unique strains of rats of which one strain (sensitive or S strain) develops severe hypertension after a variety of insults to which the other strain (resistant or R strain) responds only mildly, if at all. Our overall objectives are to define the mechanisms critical in determining the differences between strains in this susceptibility to hypertension. An extensive genetic study clearly demonstrated that these differences were multigenic in origin. This implies, of course, that to search for a single cause of hypertension is an oversimplification. We proposed to study animals from these two strains as follows: 1) study the effect of R and S renal homografts on the paradoxical response of salt-fed parabionts in which an R rat, united with an S rat, rapidly developed hypertension to higher levels and earlier than S rats; 2) begin a study on the effect of peripheral sympathectomy on salt-induced and stress-induced hypertension; 3) initiate a study on the effects of central sympathectomy on salt-induced and stress-induced hypertension; 4) continue efforts to isolate and characterize the humoral factors other than renin originating in kidneys of S rats.